The objective was to extend our data base to include the effects of an in vivo ethanol exposure paradigm on vascular reactivity with particular reference to the involvement of the prostaglandin system in such effects. The design and setup of inhalation chambers and a monitor/control apparatus for an ethanol vapor exposure paradigm has allowed us to examine the cardiovascular consequences of graded blood ethanol concentrations (BEC) during acute and chronic exposure periods. For this purpose, (1) a smooth muscle bath system was set up to measure reactivity of isolated vasculature, using force displacement transducers, and (2) a harness and tether system was set up in order to maintain a cannula in ambulatory rats while measuring changes in blood pressure (systemic arterial pressure) and its reactivity, using pressure transducers. Our in vitro results in the rat aorta, following either short-term (1-day) or long-term (14-day) exposure to ethanol vapor, show a biphasic response with regard to the contractile response to a thromboxane-mimic; moderate BEC decreased contractility, whereas high levels had no effect. Similarly treated rats showed a marked increase in the PGI-2/TXA-2 ratio, due primarily to increased PGI-2 levels, which coincided with a depression in contractility. PGI-2 levels were not affected in aorta obtained from rats with high BEC. Chronic exposure to ethanol vapor resulted in a similar PGI-2/TXA-2 ratio but lower absolute levels of these prostaglandins, which may have resulted from arachidonate depletion. Preliminary studies indicate that blood pressure and its reactivity is related to the BEC in these rats. Acute exposure to physiologically tolerable BEC depressed blood pressure and was directly related to the time of exposure of ethanol vapors. However, the BP of high-salt rats increased after 6 days of ethanol exposure. Vasoreactivity was enhanced in normal rats following a similar exposure to ethanol vapors; both vasopressor and vasodepressor effects were markedly potentiated.